Y-chromosome loss is frequent in male renal tumors.
Y-loss
fluorescence in-situ hybridization (FISH)
prognosis
renal cell neoplasm
Journal
Annals of translational medicine
ISSN: 2305-5839
Titre abrégé: Ann Transl Med
Pays: China
ID NLM: 101617978
Informations de publication
Date de publication:
Feb 2021
Feb 2021
Historique:
entrez:
12
3
2021
pubmed:
13
3
2021
medline:
13
3
2021
Statut:
ppublish
Résumé
Loss of the Y-chromosome is a common event in different tumor types but its prevalence and clinical relevance in renal cell tumors is still not understood. It was the aim of this study to estimate the frequency and clinical relevance of Y-loss in kidney neoplasms. A cohort of 1,252 male renal tumors was analyzed in a tissue microarray format by fluorescence in-situ hybridization (FISH). Y-loss was found in 47% of tumors. The frequency of this alteration varied markedly between kidney tumor subtypes. Y-loss was most prevalent in papillary renal cell carcinoma (RCC) (77%) followed by chromophobe RCC (60%), oncocytoma (51%), clear cell RCC (39%) and clear cell (tubulo)papillary RCC (19%). Y-loss was linked to higher patient age and smaller tumor size at diagnosis. Mean age (95% CI) was 65 (64-66) years in patients with Y-loss in their tumor compared to 60 (58-61) years in patients without Y-loss (P<0.0001). Significant correlations between Y-loss and tumor phenotype were found only for papillary carcinomas (P=0.002), especially for type 1 (P=0.03). Y-loss is present in different histologic subtypes of renal neoplasm. The highest frequency is in papillary RCC, where it may represent a potentially relevant prognostic biomarker suggesting favorable disease outcome.
Sections du résumé
BACKGROUND
BACKGROUND
Loss of the Y-chromosome is a common event in different tumor types but its prevalence and clinical relevance in renal cell tumors is still not understood.
METHODS
METHODS
It was the aim of this study to estimate the frequency and clinical relevance of Y-loss in kidney neoplasms. A cohort of 1,252 male renal tumors was analyzed in a tissue microarray format by fluorescence in-situ hybridization (FISH).
RESULTS
RESULTS
Y-loss was found in 47% of tumors. The frequency of this alteration varied markedly between kidney tumor subtypes. Y-loss was most prevalent in papillary renal cell carcinoma (RCC) (77%) followed by chromophobe RCC (60%), oncocytoma (51%), clear cell RCC (39%) and clear cell (tubulo)papillary RCC (19%). Y-loss was linked to higher patient age and smaller tumor size at diagnosis. Mean age (95% CI) was 65 (64-66) years in patients with Y-loss in their tumor compared to 60 (58-61) years in patients without Y-loss (P<0.0001). Significant correlations between Y-loss and tumor phenotype were found only for papillary carcinomas (P=0.002), especially for type 1 (P=0.03).
CONCLUSIONS
CONCLUSIONS
Y-loss is present in different histologic subtypes of renal neoplasm. The highest frequency is in papillary RCC, where it may represent a potentially relevant prognostic biomarker suggesting favorable disease outcome.
Identifiants
pubmed: 33708836
doi: 10.21037/atm-20-3061
pii: atm-09-03-209
pmc: PMC7940894
doi:
Types de publication
Journal Article
Langues
eng
Pagination
209Informations de copyright
2021 Annals of Translational Medicine. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/atm-20-3061). The authors have no conflicts of interest to declare.
Références
Prostate. 2012 Jun 1;72(8):898-903
pubmed: 21956681
N Engl J Med. 2012 Mar 8;366(10):883-892
pubmed: 22397650
Clin Lab Haematol. 1999 Feb;21(1):17-20
pubmed: 10197258
Cancer Genet Cytogenet. 1995 Jul 15;82(2):163-9
pubmed: 7664248
Cancer Res. 2004 Dec 1;64(23):8534-40
pubmed: 15574759
Am J Surg Pathol. 1982 Oct;6(7):655-63
pubmed: 7180965
Chin Med J (Engl). 2007 Nov 20;120(22):2002-5
pubmed: 18067786
Methods Mol Biol. 2010;664:113-26
pubmed: 20690058
Int J Cancer. 2006 May 1;118(9):2190-4
pubmed: 16331604
Int J Cancer. 2002 Apr 1;98(4):532-8
pubmed: 11920612
Cancer Res. 1994 Aug 15;54(16):4472-80
pubmed: 8044798
Cancer Genet Cytogenet. 2007 Oct 1;178(1):26-35
pubmed: 17889705
Head Neck. 2019 Apr;41(4):993-1006
pubmed: 30582241
Pathol Res Pract. 1986 May;181(2):125-43
pubmed: 3737468
Oncol Rep. 2005 May;13(5):949-56
pubmed: 15809763
World J Urol. 2015 Oct;33(10):1561-9
pubmed: 25527909
Cancer Genet Cytogenet. 1995 Dec;85(2):152-4
pubmed: 8548740
Am J Surg Pathol. 2013 Oct;37(10):1469-89
pubmed: 24025519
Genes Chromosomes Cancer. 1993 Nov;8(3):172-7
pubmed: 7509625
Pathology. 2010 Jun;42(4):356-9
pubmed: 20438408
Virchows Arch. 2008 Oct;453(4):313-9
pubmed: 18795325
Am J Hum Genet. 2016 Jun 2;98(6):1208-1219
pubmed: 27231129
Anticancer Res. 2006 Jan-Feb;26(1A):319-23
pubmed: 16475713
Leuk Res. 2017 Dec;63:85-89
pubmed: 29121539
J Thorac Oncol. 2019 Jan;14(1):37-44
pubmed: 30267841
Am J Pathol. 2000 Feb;156(2):555-66
pubmed: 10666385
Int J Cancer. 2013 Jun 15;132(12):2948-55
pubmed: 23180689
Oncogene. 2013 Oct;32(40):4727-36
pubmed: 23318433
Am J Hum Genet. 1995 Nov;57(5):1143-50
pubmed: 7485166
Clin Lymphoma Myeloma Leuk. 2017 Mar;17(3):159-164.e2
pubmed: 28089441
PLoS One. 2016 Jan 08;11(1):e0146264
pubmed: 26745889
Am J Pathol. 2001 Jun;158(6):1961-7
pubmed: 11395372
Histopathology. 2000 Sep;37(3):241-9
pubmed: 10971700
Mod Pathol. 2003 Oct;16(10):1060-3
pubmed: 14559991
Nat Genet. 2014 Jun;46(6):624-8
pubmed: 24777449
Mod Pathol. 2008 Nov;21(11):1371-8
pubmed: 18552821
Hum Pathol. 2017 Mar;61:210-220
pubmed: 28025079
Arch Pathol Lab Med. 2008 Aug;132(8):1329-32
pubmed: 18684036
Am J Pathol. 1999 Apr;154(4):981-6
pubmed: 10233835
Genes Chromosomes Cancer. 1991 Jul;3(4):249-55
pubmed: 1958590
Cancer Res. 1997 Jul 1;57(13):2765-80
pubmed: 9205089
Am J Pathol. 2001 Dec;159(6):2249-56
pubmed: 11733374
J Urol. 2004 Feb;171(2 Pt 1):602-4
pubmed: 14713769
J Clin Oncol. 2009 Feb 10;27(5):746-53
pubmed: 19124809
Am J Pathol. 1994 Aug;145(2):356-64
pubmed: 7519827
Genes Chromosomes Cancer. 1993 Jan;6(1):58-60
pubmed: 7680223